In vivo stimulation-induced release of manganese in rat amygdala

Takeda, Atsüshi; Ishiwatari, Shioji; Okada, Shoji

doi:10.1016/s0006-8993(98)00881-6

Cited by 43 publications

(26 citation statements)

References 14 publications

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“…Mn deficiency and the ensuing low Mn concentration in the blood are known to be associated with epilepsy in both humans and experimental animals (Carl et al, 1993). Moreover, Mn ions may be involved in the processes dynamically coupled to the electrophysiological activity of neuronal axons; we demonstrated that Mn is released with neurotransmitters into the extracellular space during stimulation with high K ϩ (Takeda et al, 1998d).…”

Section: Introductionmentioning

confidence: 67%

“…Mn is subject to widespread axonal transport in the neural circuits within the brain (Sloot and Gramsbergen, 1994) and may be transported to post-synaptic neurons via the synapse (Takeda et al, 1998b). Recently we demonstrated that Mn is released with neurotransmitters into the extracellular space during stimulation with high K ϩ (Takeda et al, 1998d). Mn ions may be involved in the processes dynamically coupled to the electrophysiological activity of neuronal axons.…”

Section: Discussionmentioning

confidence: 99%

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Manganese uptake into rat brain during development and aging

1999

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Manganese (Mn) is an essential metal and plays an important role in the brain. To evaluate Mn uptake into the brain during development and aging, 54Mn concentrations in the brain of rats aged from 5 days to 95 weeks were measured after injection of 54MnCl2. 54Mn concentration in the brain of 5-day-old rats was the highest of all age groups tested. The liver and blood of 5-day-old rats also showed the highest 54Mn concentrations among the age groups. These results suggest that Mn is required in a high amount during infancy and that a sufficient Mn supply is critical for normal brain development. The high uptake of Mn into the brain of neonatal rats may be due to high levels of Mn in the blood, which may be supplied from the liver. In the 5-day-old brain, 54Mn was relatively concentrated in the hippocampal CA3 and dentate gyrus and the pons. In the aging brain, 54Mn was relatively concentrated in the inferior colliculi, olivary nuclei and red nuclei.

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Section: Introductionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Manganese uptake into rat brain during development and aging

1999

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“…Furthermore, blockage of the retinal ganglion cell activity by intravitrial co-injection of the sodium channel blocker tetrodotoxin failed to reduce the manganese-induced signal enhancement in the superior colliculus (171). However, electrical activity seems to be required for synaptic transmission (161), where manganese is released together with neurotransmitters as shown by 54 Mn (172). Transsynaptic manganese transport is reduced by isoflurane, which is known to depress the action potential and vesicular release at the pre-synaptic site, and by a blockage of the post-synaptic NMDA-receptor (41).…”

Section: Physiological Basismentioning

confidence: 99%

Manganese-Enhanced Magnetic Resonance Imaging

Boretius

Frahm

2011

Methods in Molecular Biology

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Manganese-enhanced magnetic resonance imaging (MEMRI) relies on contrasts that are due to the shortening of the T (1) relaxation time of tissue water protons that become exposed to paramagnetic manganese ions. In experimental animals, the technique combines the high spatial resolution achievable by MRI with the biological information gathered by tissue-specific or functionally induced accumulations of manganese. After in vivo administration, manganese ions may enter cells via voltage-gated calcium channels. In the nervous system, manganese ions are actively transported along the axon. Based on these properties, MEMRI is increasingly used to delineate neuroanatomical structures, assess differences in functional brain activity, and unravel neuronal connectivities in both healthy animals and models of neurological disorders. Because of the cellular toxicity of manganese, a major challenge for a successful MEMRI study is to achieve the lowest possible dose for a particular biological question. Moreover, the interpretation of MEMRI findings requires a profound knowledge of the behavior of manganese in complex organ systems under physiological and pathological conditions. Starting with an overview of manganese pharmacokinetics and mechanisms of toxicity, this chapter covers experimental methods and protocols for applications in neuroscience.

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“…Further, a number of studies suggest that the uptake and/or transport of manganese to specific terminal fields may be activity dependent (8,12,13). Similarly, the co-release of manganese with glutamate (14) suggests that trans-synaptic release into secondary terminal fields may also be activity dependent. With an average speed of anterograde transport of 2.8 mm/h (6) and the time required to accumulate sufficient label for visualisation with MRI, the labelling time for most putative pathways of interest is considerable.…”

Section: Introductionmentioning

confidence: 99%

Quantitative manganese tract tracing: dose‐dependent and activity‐independent terminal labelling in the mouse visual system

Lowe¹,

Thompson

Sibson³

2008

NMR in Biomedicine

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At concentrations sufficient for visualisation using MRI, manganese (Mn) is believed to behave as a calcium analogue. This study examines different concentrations of Mn for enhanced MR tract tracing. The premise of activity-dependent axonal transport was also examined by partial or complete blockade of retinal ganglion cell activity. Quantitative T(1) maps and semi-quantitative normalised signal intensities in the superior colliculi facilitated assessment of applied intraocular concentrations and activity dependence, respectively. Varying the concentration of applied Mn revealed a non-monotonic profile, with optimal, unfavourable and undesirable effects noted: 25 mM proved optimal, showing a maximal decrease in T(1), whereas 400 mM was associated with no terminal-field enhancement. The estimated vitreal concentration for optimal transport of Mn (2 mM) is substantially lower than that used in previous studies of the mouse. Both the partial blockade of inputs to 50% of retinal ganglion cells by a mGluR6 glutamate agonist and the complete blockade of all retinal ganglion cell activity with tetrodotoxin failed to decrease the relative enhancement in the superior colliculus. The failure to prevent axonal transport of Mn by blocking activity (and therefore theoretically the intracellular influx) appeared to be paradoxical. The optimal vitreal concentration of Mn has previously been shown to facilitate massive intracellular uptake of Mn, competitively blocking calcium, and 1 mM Mn blocks neurotransmission pre-synaptically. These results suggest that, at concentrations required for optimal Mn-enhanced MRI tract tracing in the visual system of the mouse, the uptake and transport of Mn may be dominated by passive mechanisms, which may also block neurotransmission.

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In vivo stimulation-induced release of manganese in rat amygdala

Cited by 43 publications

References 14 publications

Manganese uptake into rat brain during development and aging

Manganese uptake into rat brain during development and aging

Manganese-Enhanced Magnetic Resonance Imaging

Quantitative manganese tract tracing: dose‐dependent and activity‐independent terminal labelling in the mouse visual system

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